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  • 1
    Publication Date: 2012-09-08
    Description: Eukaryotic cells make many types of primary and processed RNAs that are found either in specific subcellular compartments or throughout the cells. A complete catalogue of these RNAs is not yet available and their characteristic subcellular localizations are also poorly understood. Because RNA represents the direct output of the genetic information encoded by genomes and a significant proportion of a cell's regulatory capabilities are focused on its synthesis, processing, transport, modification and translation, the generation of such a catalogue is crucial for understanding genome function. Here we report evidence that three-quarters of the human genome is capable of being transcribed, as well as observations about the range and levels of expression, localization, processing fates, regulatory regions and modifications of almost all currently annotated and thousands of previously unannotated RNAs. These observations, taken together, prompt a redefinition of the concept of a gene.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3684276/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3684276/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Djebali, Sarah -- Davis, Carrie A -- Merkel, Angelika -- Dobin, Alex -- Lassmann, Timo -- Mortazavi, Ali -- Tanzer, Andrea -- Lagarde, Julien -- Lin, Wei -- Schlesinger, Felix -- Xue, Chenghai -- Marinov, Georgi K -- Khatun, Jainab -- Williams, Brian A -- Zaleski, Chris -- Rozowsky, Joel -- Roder, Maik -- Kokocinski, Felix -- Abdelhamid, Rehab F -- Alioto, Tyler -- Antoshechkin, Igor -- Baer, Michael T -- Bar, Nadav S -- Batut, Philippe -- Bell, Kimberly -- Bell, Ian -- Chakrabortty, Sudipto -- Chen, Xian -- Chrast, Jacqueline -- Curado, Joao -- Derrien, Thomas -- Drenkow, Jorg -- Dumais, Erica -- Dumais, Jacqueline -- Duttagupta, Radha -- Falconnet, Emilie -- Fastuca, Meagan -- Fejes-Toth, Kata -- Ferreira, Pedro -- Foissac, Sylvain -- Fullwood, Melissa J -- Gao, Hui -- Gonzalez, David -- Gordon, Assaf -- Gunawardena, Harsha -- Howald, Cedric -- Jha, Sonali -- Johnson, Rory -- Kapranov, Philipp -- King, Brandon -- Kingswood, Colin -- Luo, Oscar J -- Park, Eddie -- Persaud, Kimberly -- Preall, Jonathan B -- Ribeca, Paolo -- Risk, Brian -- Robyr, Daniel -- Sammeth, Michael -- Schaffer, Lorian -- See, Lei-Hoon -- Shahab, Atif -- Skancke, Jorgen -- Suzuki, Ana Maria -- Takahashi, Hazuki -- Tilgner, Hagen -- Trout, Diane -- Walters, Nathalie -- Wang, Huaien -- Wrobel, John -- Yu, Yanbao -- Ruan, Xiaoan -- Hayashizaki, Yoshihide -- Harrow, Jennifer -- Gerstein, Mark -- Hubbard, Tim -- Reymond, Alexandre -- Antonarakis, Stylianos E -- Hannon, Gregory -- Giddings, Morgan C -- Ruan, Yijun -- Wold, Barbara -- Carninci, Piero -- Guigo, Roderic -- Gingeras, Thomas R -- 062023/Wellcome Trust/United Kingdom -- 1RC2HG005591/HG/NHGRI NIH HHS/ -- 249968/European Research Council/International -- P30 CA045508/CA/NCI NIH HHS/ -- R01 HG003700/HG/NHGRI NIH HHS/ -- R01HG003700/HG/NHGRI NIH HHS/ -- R37 GM062534/GM/NIGMS NIH HHS/ -- RC2 HG005591/HG/NHGRI NIH HHS/ -- U01 HG003147/HG/NHGRI NIH HHS/ -- U54 HG004555/HG/NHGRI NIH HHS/ -- U54 HG004557/HG/NHGRI NIH HHS/ -- U54 HG004558/HG/NHGRI NIH HHS/ -- U54 HG004576/HG/NHGRI NIH HHS/ -- U54 HG007004/HG/NHGRI NIH HHS/ -- U54HG004555/HG/NHGRI NIH HHS/ -- U54HG004557/HG/NHGRI NIH HHS/ -- U54HG004558/HG/NHGRI NIH HHS/ -- U54HG004576/HG/NHGRI NIH HHS/ -- England -- Nature. 2012 Sep 6;489(7414):101-8. doi: 10.1038/nature11233.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Genomic Regulation and UPF, Doctor Aiguader 88, Barcelona 08003, Catalonia, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22955620" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Cell Line ; DNA/*genetics ; DNA, Intergenic/genetics ; *Encyclopedias as Topic ; Enhancer Elements, Genetic ; Exons/genetics ; Gene Expression Profiling ; Genes/genetics ; Genome, Human/*genetics ; Genomics ; Humans ; *Molecular Sequence Annotation ; Polyadenylation/genetics ; Protein Isoforms/genetics ; RNA/biosynthesis/genetics ; RNA Editing/genetics ; RNA Splicing/genetics ; Regulatory Sequences, Nucleic Acid/*genetics ; Repetitive Sequences, Nucleic Acid/genetics ; Sequence Analysis, RNA ; Transcription, Genetic/*genetics ; Transcriptome/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2013-11-12
    Description: In multicellular organisms, transcription regulation is one of the central mechanisms modelling lineage differentiation and cell-fate determination. Transcription requires dynamic chromatin configurations between promoters and their corresponding distal regulatory elements. It is believed that their communication occurs within large discrete foci of aggregated RNA polymerases termed transcription factories in three-dimensional nuclear space. However, the dynamic nature of chromatin connectivity has not been characterized at the genome-wide level. Here, through a chromatin interaction analysis with paired-end tagging approach using an antibody that primarily recognizes the pre-initiation complexes of RNA polymerase II, we explore the transcriptional interactomes of three mouse cells of progressive lineage commitment, including pluripotent embryonic stem cells, neural stem cells and neurosphere stem/progenitor cells. Our global chromatin connectivity maps reveal approximately 40,000 long-range interactions, suggest precise enhancer-promoter associations and delineate cell-type-specific chromatin structures. Analysis of the complex regulatory repertoire shows that there are extensive colocalizations among promoters and distal-acting enhancers. Most of the enhancers associate with promoters located beyond their nearest active genes, indicating that the linear juxtaposition is not the only guiding principle driving enhancer target selection. Although promoter-enhancer interactions exhibit high cell-type specificity, promoters involved in interactions are found to be generally common and mostly active among different cells. Chromatin connectivity networks reveal that the pivotal genes of reprogramming functions are transcribed within physical proximity to each other in embryonic stem cells, linking chromatin architecture to coordinated gene expression. Our study sets the stage for the full-scale dissection of spatial and temporal genome structures and their roles in orchestrating development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3954713/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3954713/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Yubo -- Wong, Chee-Hong -- Birnbaum, Ramon Y -- Li, Guoliang -- Favaro, Rebecca -- Ngan, Chew Yee -- Lim, Joanne -- Tai, Eunice -- Poh, Huay Mei -- Wong, Eleanor -- Mulawadi, Fabianus Hendriyan -- Sung, Wing-Kin -- Nicolis, Silvia -- Ahituv, Nadav -- Ruan, Yijun -- Wei, Chia-Lin -- 1U54HG004557-01/HG/NHGRI NIH HHS/ -- GGP12152/Telethon/Italy -- GM61390/GM/NIGMS NIH HHS/ -- R01 DK090382/DK/NIDDK NIH HHS/ -- R01 HD059862/HD/NICHD NIH HHS/ -- R01 HG004456-01/HG/NHGRI NIH HHS/ -- R01 NS079231/NS/NINDS NIH HHS/ -- R01DK090382/DK/NIDDK NIH HHS/ -- R01HD059862/HD/NICHD NIH HHS/ -- R01HG003521-01/HG/NHGRI NIH HHS/ -- R01HG005058/HG/NHGRI NIH HHS/ -- R01HG006768/HG/NHGRI NIH HHS/ -- R01NS079231/NS/NINDS NIH HHS/ -- U01 GM061390/GM/NIGMS NIH HHS/ -- U19 GM061390/GM/NIGMS NIH HHS/ -- England -- Nature. 2013 Dec 12;504(7479):306-10. doi: 10.1038/nature12716. Epub 2013 Nov 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Sequencing Technology Group, Joint Genome Institute, Lawrence Berkeley National Laboratory, Walnut Creek, California 94598, USA [2] [3] Department of Life Sciences, Faculty of Natural Sciences, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel (R.Y.B.); National Heart, Lung, and Blood Institute, National Institutes of Health, Systems Biology Center, 9000 Rockville Pike, Bethesda, Maryland 20892, USA (Y.Z.). ; 1] Sequencing Technology Group, Joint Genome Institute, Lawrence Berkeley National Laboratory, Walnut Creek, California 94598, USA [2]. ; 1] Department of Bioengineering and Therapeutic Sciences, Institute for Human Genetics, UCSF, San Francisco, California 94158, USA [2] [3] Department of Life Sciences, Faculty of Natural Sciences, Ben-Gurion University of the Negev, Beer-Sheva 8410501, Israel (R.Y.B.); National Heart, Lung, and Blood Institute, National Institutes of Health, Systems Biology Center, 9000 Rockville Pike, Bethesda, Maryland 20892, USA (Y.Z.). ; 1] The Jackson Laboratory for Genomic Medicine, and Department of Genetic and Development Biology, University of Connecticut, 400 Farmington, Connecticut 06030, USA [2] Genome Institute of Singapore, 60 Biopolis Street, 138672 Singapore. ; Department of Biological Sciences and Biotechnology, University of Milano-Bicocca, 20126 Milano, Italy. ; Sequencing Technology Group, Joint Genome Institute, Lawrence Berkeley National Laboratory, Walnut Creek, California 94598, USA. ; Genome Institute of Singapore, 60 Biopolis Street, 138672 Singapore. ; Department of Bioengineering and Therapeutic Sciences, Institute for Human Genetics, UCSF, San Francisco, California 94158, USA. ; The Jackson Laboratory for Genomic Medicine, and Department of Genetic and Development Biology, University of Connecticut, 400 Farmington, Connecticut 06030, USA. ; 1] Sequencing Technology Group, Joint Genome Institute, Lawrence Berkeley National Laboratory, Walnut Creek, California 94598, USA [2] Genome Institute of Singapore, 60 Biopolis Street, 138672 Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24213634" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cell Lineage ; Chromatin/*genetics/*metabolism ; Embryonic Stem Cells/metabolism ; Enhancer Elements, Genetic/*genetics ; Gene Expression Regulation/*genetics ; In Situ Hybridization, Fluorescence ; Mice ; Neural Stem Cells/metabolism ; Promoter Regions, Genetic/*genetics ; RNA Polymerase II/metabolism ; Transcription, Genetic/genetics ; Zebrafish/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2015-02-18
    Description: Enhancers regulate spatiotemporal gene expression and impart cell-specific transcriptional outputs that drive cell identity. Super-enhancers (SEs), also known as stretch-enhancers, are a subset of enhancers especially important for genes associated with cell identity and genetic risk of disease. CD4(+) T cells are critical for host defence and autoimmunity. Here we analysed maps of mouse T-cell SEs as a non-biased means of identifying key regulatory nodes involved in cell specification. We found that cytokines and cytokine receptors were the dominant class of genes exhibiting SE architecture in T cells. Nonetheless, the locus encoding Bach2, a key negative regulator of effector differentiation, emerged as the most prominent T-cell SE, revealing a network in which SE-associated genes critical for T-cell biology are repressed by BACH2. Disease-associated single-nucleotide polymorphisms for immune-mediated disorders, including rheumatoid arthritis, were highly enriched for T-cell SEs versus typical enhancers or SEs in other cell lineages. Intriguingly, treatment of T cells with the Janus kinase (JAK) inhibitor tofacitinib disproportionately altered the expression of rheumatoid arthritis risk genes with SE structures. Together, these results indicate that genes with SE architecture in T cells encompass a variety of cytokines and cytokine receptors but are controlled by a 'guardian' transcription factor, itself endowed with an SE. Thus, enumeration of SEs allows the unbiased determination of key regulatory nodes in T cells, which are preferentially modulated by pharmacological intervention.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4409450/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4409450/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vahedi, Golnaz -- Kanno, Yuka -- Furumoto, Yasuko -- Jiang, Kan -- Parker, Stephen C J -- Erdos, Michael R -- Davis, Sean R -- Roychoudhuri, Rahul -- Restifo, Nicholas P -- Gadina, Massimo -- Tang, Zhonghui -- Ruan, Yijun -- Collins, Francis S -- Sartorelli, Vittorio -- O'Shea, John J -- 105663/Z/14/Z/Wellcome Trust/United Kingdom -- R01 CA186714/CA/NCI NIH HHS/ -- ZIA AR041159-07/Intramural NIH HHS/ -- England -- Nature. 2015 Apr 23;520(7548):558-62. doi: 10.1038/nature14154. Epub 2015 Feb 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Cell Biology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland 20892, USA. ; Translational Immunology Section, NIAMS, NIH, Bethesda, Maryland 20892, USA. ; Medical Genomics and Metabolic Genetics Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland 20892, USA. ; Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA. ; The Jackson Laboratory for Genomic Medicine and Department of Genetic and Development Biology, University of Connecticut, Farmington, Connecticut 06030, USA. ; Laboratory of Muscle Stem Cells and Gene Regulation, NIAMS, NIH, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25686607" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/*genetics/immunology/pathology ; Basic-Leucine Zipper Transcription Factors/metabolism ; Cell Differentiation/genetics ; Cell Lineage/genetics ; Enhancer Elements, Genetic/*genetics ; Gene Expression Regulation/genetics ; Genetic Predisposition to Disease/genetics ; Janus Kinase 3/antagonists & inhibitors ; Mice ; Mice, Inbred C57BL ; Piperidines/pharmacology ; Pyrimidines/pharmacology ; Pyrroles/pharmacology ; RNA, Untranslated/genetics ; T-Lymphocytes, Helper-Inducer/immunology/*metabolism/*pathology ; Transcription, Genetic/genetics ; p300-CBP Transcription Factors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2011-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruan, Yijun -- New York, N.Y. -- Science. 2011 Feb 25;331(6020):1025-6. doi: 10.1126/science.1203602.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genome Institute of Singapore, Singapore, Republic of Singapore.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350163" target="_blank"〉PubMed〈/a〉
    Keywords: Chromatin/*ultrastructure ; Chromosomes, Human/*ultrastructure ; *Genome, Human ; Human Genome Project ; Humans
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2018-02-23
    Keywords: Myeloid Neoplasia
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 6
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    German Medical Science; Düsseldorf, Köln
    In:  International Conference on SARS - one year after the (first) outbreak; 20040508-20040511; Lübeck; DOC04sars4.02 /20040526/
    Publication Date: 2004-05-26
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 7
    ISSN: 0378-1119
    Keywords: Nectria ; RNA polymerase II ; fungal promoter ; gene regulation
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Geometric and functional analysis 3 (1993), S. 395-430 
    ISSN: 1420-8970
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1617-4623
    Keywords: Key wordsZea mays ; Sucrose synthase ; Isozymes ; Cellulose biosynthesis ; Starch biosynthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In maize, two paralogous genes, Sh1 and Sus1, encode two biochemically similar isozymes of sucrose synthase, SS1 and SS2, respectively. Previous studies have attributed the mild starch deficiency of the shrunken1 (sh1) endosperm to the loss of the SS1 isozyme in the mutant. Here we describe the first mutation in the sucrose synthase1 (Sus1) gene, sus1-1, and the isolation of a double recessive genotype, sh1 sus1-1. Combined data from diverse studies, including Northern and Western analyses, RT-PCR and genomic PCR, cloning and sequencing data for the 3′ region, show that the mutant sus1-1 gene has a complex pattern of expression, albeit at much reduced levels as compared to the Sus1 gene. Endosperm sucrose synthase activity in sh1 sus1-1 was barely 0.5% of the total activity in the Sh1 Sus1 genotype. Significantly, comparative analyses of Sh1 Sus1, sh1 Sus1 and sh1 sus1-1 genotypes have, for the first time, allowed us to dissect the relative contributions of each isozyme to endosperm development. Starch contents in endosperm of the three related genotypes were 100, 78 and 53%, respectively. Anatomical analyses, which confirmed the previously described early cell degeneration phenotype unique to the sh1 Sus1 endosperm, revealed no detectable difference between the two sh1 genotypes. We conclude that the SS1 isozyme plays the dominant role in providing the substrate for cellulose biosynthesis, whereas the SS2 protein is needed mainly for generating precursors for starch biosynthesis.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1617-4623
    Keywords: Key words Phytoalexin degradation ; Plant-pathogen interactions ; Plant flavonoid ; Transcriptional activator
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  Expression of the PDA1 gene in the ascomycete Nectria haematococca MPVI (anamorph: Fusarium solani) is induced by exposure of mycelium to pisatin, an isoflavonoid phytoalexin produced by its host plant, garden pea. The PDA1 gene encodes a cytochrome P-450 monooxygenase which detoxifies pisatin. Regulatory elements controlling transcription from the PDA1 promoter were identified using a homologous Nectria in vitro transcription system through analysis of 5′ deletions, specific oligonucleotide competition, and fusion of upstream segments to a heterologous promoter. A promoter-distal element which provided transcriptional activation was localized to a 35-bp region positioned −514 to −483 upstream of the transcriptional start site. This 35-bp region binds a previously characterized pisatin-responsive DNA-binding factor (PRF) and thus may provide pisatin-responsive control of transcription. A second promoter-proximal positive-acting region was found to be necessary for promoter transcription in both homologous and heterologous extracts, and so is likely to bind less gene-specific transcription activator(s). A negative-acting element located between these two positive regions may act to make the positive-acting elements interdependent. The identification of an activator responding to pisatin provides a model for the control of a number of genes and processes controlled by host-specific signals, particularly the flavonoids.
    Type of Medium: Electronic Resource
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